Increased expression of long non-coding RNA FIRRE promotes hepatocellular carcinoma by HuR-CyclinD1 axis signaling.
Autor: | Haga Y; Department of Internal Medicine, Saint Louis University, St. Louis, Missouri, USA., Bandyopadhyay D; Department of Pathology, Saint Louis University, St. Louis, Missouri, USA., Khatun M; Department of Pathology, Saint Louis University, St. Louis, Missouri, USA., Tran E; Department of Pathology, Saint Louis University, St. Louis, Missouri, USA., Steele R; Department of Pathology, Saint Louis University, St. Louis, Missouri, USA., Banerjee S; Department of Pathology, Saint Louis University, St. Louis, Missouri, USA., Ray R; Department of Internal Medicine, Saint Louis University, St. Louis, Missouri, USA., Nazzal M; Department of Surgery, Saint Louis University, St. Louis, Missouri, USA., Ray RB; Department of Pathology, Saint Louis University, St. Louis, Missouri, USA. Electronic address: ratna.ray@health.slu.edu. |
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Jazyk: | angličtina |
Zdroj: | The Journal of biological chemistry [J Biol Chem] 2024 May; Vol. 300 (5), pp. 107247. Date of Electronic Publication: 2024 Mar 29. |
DOI: | 10.1016/j.jbc.2024.107247 |
Abstrakt: | There is a critical need to understand the disease processes and identify improved therapeutic strategies for hepatocellular carcinoma (HCC). The long noncoding RNAs (lncRNAs) display diverse effects on biological regulations. The aim of this study was to identify a lncRNA as a potential biomarker of HCC and investigate the mechanisms by which the lncRNA promotes HCC progression using human cell lines and in vivo. Using RNA-Seq analysis, we found that lncRNA FIRRE was significantly upregulated in hepatitis C virus (HCV) associated liver tissue and identified that lncRNA FIRRE is significantly upregulated in HCV-associated HCC compared to adjacent non-tumor liver tissue. Further, we observed that FIRRE is significantly upregulated in HCC specimens with other etiologies, suggesting this lncRNA has the potential to serve as an additional biomarker for HCC. Overexpression of FIRRE in hepatocytes induced cell proliferation, colony formation, and xenograft tumor formation as compared to vector-transfected control cells. Using RNA pull-down proteomics, we identified HuR as an interacting partner of FIRRE. We further showed that the FIRRE-HuR axis regulates cyclin D1 expression. Our mechanistic investigation uncovered that FIRRE is associated with an RNA-binding protein HuR for enhancing hepatocyte growth. Together, these findings provide molecular insights into the role of FIRRE in HCC progression. Competing Interests: Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article. (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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